The heart is a major target organ of thyroid hormone action. disturbances of cardiac function occur frequently in patients with diseases of the thyroid gland. In order to gain insight into the molecular basis of the cardiac atrophy of hypothyroidism and the cardiac hypertrophy of hyperthyroidism, relative synthesis rates of specific cardiac proteins and the composition of cardiac mRNA will be examined in rats of different thyroid status. Proteins formed in vivo and proteins synthesized in vitro by translation of mRNA in a heterologous protein synthesizing system will be separated by two-dimensional gel electrophoresis and quantitated. It has been shown that hypothyroidism leads to a decrease in cardiac contractility which is accompanied by a decrease in the activity of CA++ activated myosin ATPase. Recent reports and our preliminary findings indicate that three components of myosin (M-V1, M-V2, M-V3) occur in the rat ventricle. M-V1 has the highest and M-V3 the lowest specific activity of CA++ activated myosin ATPase. Myosin V1 is composed of two identical myosin heavy chains (MHC-V1), myosin V2 of one MHC-V1 and one MHC-V3, and myosin V3 is composed of two identical MHC-V3. Changes in thyroid status lead to alterations in the predominance of myosin components, M-V1 predominating in the hyperthyroid and M-V3 predominating in the hypothyroid heart. We want to confirm that the myosin components are true isoenzymes and determine if changes in isoenzyme predominance are cuased by alterations in MHC-V1 and MHC-V3 synthesis rate. Changes in MHC-V1 and MHC-V3 synthesis rate may be mediated by alterations in MHC-V1 mRNA and MHC-V3 mRNA levels. To determine this, RNA will be isolated and translated in vitro to form MHC-V1 and MHC-V3. MHC-V1 and MHC-V3 will then be quantitated by electrophorectic techniques. Patients who are chronically ill have frequently a marked decrease in their plasma T3 values but appear grossly euthyroid. This entity is called "low T3 syndrome". In order to gain insight into the molecular basis of the low T3 syndrome, plasma T3 levels, the nuclear T3 content, and specific thyroid hormone responsive tissue parameters will be determined in the heart and skeletal muscles of semi-starved rats.